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Efficacy of salbutamol and ipratropium bromide in decreasing bronchial hyperreactivity in children with cystic fibrosis
Author(s) -
Avital Avi,
Sanchez Ignacio,
Chernick Victor
Publication year - 1992
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950130109
Subject(s) - ipratropium bromide , salbutamol , medicine , methacholine , bronchodilator , anesthesia , inhalation , saline , ipratropium , asthma , respiratory disease , lung
A proportion of patients with cystic fibrosis (CF) suffer from increased airway hyperreactivity but their response to bronchodilators is variable. Adrenergic agents may produce an increase, no change or a decrease in forced expiratory volume in 1 second (FEV 1 ). We hypothesized that the variable response might be related to poor aerosol distribution caused by the presence of secretions. Therefore, in 11 children with CF and airway hyperreactivity the influence of pretreatment with either 0.9% saline, salbutamol, or ipratropium bromide on the methacholine challenge test was evaluated in a double‐blind, randomized, cross‐over study. FEV 1 (mean ± S.E.) did not change following pretreatment with saline, salbutamol, or ipratropium (1.64 ± 0.22, 1.63 ± 0.16 and 1.67 ± 0.19, respectively). All patients demonstrated airway hyperreactivity with a PC 20 below 8 mg/mL (geometric mean, 0.41 mg/mL) after saline pretreatment. Salbutamol inhalation significantly increased the PC 20 to 1.24 mg/mL ( P < 0.01), but ipratropium bromide was found to be even more effective than salbutamol (PC 20 = 7.37 mg/mL) ( P < 0.0001). We conclude that the variable response to bronchodilator is not secondary to impaired aerosol distribution since ipratropium bromide effectively blocked the response to methacholine. The improvement in PC 20 without a change in baseline FEV 1 following salbutamol suggests that the adrenergic agent altered the contractile mechanism of smooth muscle. © 1992 Wiley‐Liss, Inc.